Hernandez tops micropathlec exam

Bactol in micropathlab

Sobrevega in physiolec

bug investigators

hard-working micro students

miss evidente evidently doing 'distance learning'

bacterial cell lec slide

Prokaryotes (Bacteria)
• Eubacter "True" bacteria
– human pathogens
– clinical or environmental
– one kingdom
• Archaea
– Environmental organisms
– second kingdom
Eukaryotes
• Other cell-based life e.g.
– plants
– animals
– fungi
Prokaryotic Cell (versus Eukaryotic Cell
• Not compartmentalized
• Cell membranes lack sterols (e.g. cholesterol)
• Single circular chromosome
• Ribosomal are 70S

Bacteria
• Plasmids
• Extra-chromosomal DNA
• multiple copy number
• coding pathogenesis and antibiotic
resistance factors
• bacterial replication
The Cell Envelope
Oxidative phosphorylation occurs at cell membrane
(since there are no mitochondria
The ceined: caA‪yer or glycocalyx
• usually polysaccharide
• often lost on in vitro culture
• protective in vivo
• Many bacterial cells secrete some extracellular material in the form of a capsule or a slime layer
• A slime layer is loosely associated with the bacterium and can be easily washed off

• whereas a capsule is attached tightly to the bacterium and has definite boundaries
Endospores (spores
• Dormant cell
• Produced when starved
• Resistant to adverse conditions
- high temperatures
- organic solvents
• Bacillus and Clostridium

Culture and identification of infectious agents
Taxonomy
• Defines common traits among strains for a bacterial species

• Usually genetic

• Allows development of diagnostic kits
TAXONOMY
Classification, Nomenclature, Laboratory Identification
Identification of infectious agents
in the diagnostic laboratory
• Aids treatment
• Helps antibiotic selection
• General hospital laboratory
– physiological tests
• Reference laboratories
– Genetic tests
Steps in isolation and identification
• Step 1. Streaking culture plates
�A‪yer or glycocalyx
• usually polysaccharide
• often lost on in vitro culture
• protective in vivo
• Many bacterial cells secrete some extracellular material in the form of a capsule or a slime layer
• A slime layer is loosely associated with the bacterium and can be easily washed off

• whereas a capsule is attached tightly to the bacterium and has definite boundaries
Endospores (spores
• Dormant cell
• Produced when starved
• Resistant to adverse conditions
- high temperatures
- organic solvents
• Bacillus and Clostridium

Culture and identification of infectious agents
Taxonomy
• Defines common traits among strains for a bacterial species

• Usually genetic

• Allows development of diagnostic kits
TAXONOMY
Classification, Nomenclature, Laboratory Identification
Identification of infectious agents
in the diagnostic laboratory
• Aids treatment
• Helps antibiotic selection
• General hospital laboratory
– physiological tests
• Reference laboratories
– Genetic tests
Steps in isolation and identification
• Step 1. Streaking culture plates
– colonies on incubation (e.g 24 hr)
– size, texture, color, hemolysis
– oxygen requirement
Samples of body fliuds (blood,urine,csf)
• Step 2. Colonies Gram stained
– cells observed microscopically
Gram stain morphology
• Shape
– cocci (round)
– bacilli (rods)
– spiral or curved (e.g. spirochetes)

• Single or multiple cells
– clusters (e.g. staphylococci)
– chains (e.g. streptococci)

• Gram positive or negative

Step 3. Isolated
bacteria are speciated
• Generally using physiological tests
Step 4.
Antibiotic susceptibility testing
Molecular differentiation
• Genomics

• Gene characterization
– Sequencing
– PCR

• Hybridization

• % guanine + cytosine
16S rRNA Sequencing
• Differentiates bacterial species
• Development of clinical tests based on sequence (e.g. PCR)

Rapid diagnosis without culture
• WHEN AND WHY?
• grow poorly
• can not be cultured
Microscopy
• spinal fluids (meningitis)
• sputum (tuberculosis)

• sensitivity poor
Serologic identification
• antibody response to the infecting agent

• several weeks after an infection has occurred

Nutrition, Growth and Metabolism
Bacterial requirements for growth
• oxygen (or absence)
• energy
• nutrients
• optimal temperature
• optimal pH
Respiration
• Respiration is the oxidation of a source of energy by removal of electrons and donation to an inorganic terminal electron accepter.
Fermentation
• Fermentation is defined as an energy yielding process whereby organic molecules serve as both electron donors and electron accepters

• The molecule being metabolized does not have all its potential energy extracted from it. In other words, it is not completely oxidized
Oxygen Requirements
Obligate aerobes must grow in the presence of oxygen they cannot carry out fermentation
Obligate anaerobes do not carry out oxidative phosphorylation they are killed by oxygen
Aerotolerant anaerobes are bacteria that respire anaerobically but can survive in the presence of oxygen
Facultative anaerobes can perform both fermentation and aerobic respiration
Microaerophilic bacteria grow well in low concentrations of oxygen,but are killed by higher concentrations.
Obligate aerobes
• grow in presence of oxygen
• no fermentation
• oxidative phosphorylation
Obligate anaerobes
• no oxidative phosphorylation
• fermentation
• killed by oxygen
• lack certain enzymes
superoxide dismutase
O2-+2H+ H2O2
catalase
H2O2 H20 + O2
peroxidase
H2O2 H20 /NAD NADH
Facultative anaerobes
• fermentation
• aerobic respiration
• survive in oxygen
Microaerophilic bacteria
• grow
– low oxygen
• killed
– high oxygen

Optimal growth temperature
• Mesophiles:
– human body temperature
* pathogens
* opportunists
• pyschrophile
– close to freezing
• thermophile
– close to boiling
pH
• Many grow best at neutral pH
• Some can survive/grow
- acid
- alkali
Nutrient Requirements
• Carbon
• Nitrogen
• Phosphorus
• Sulfur
• Metal ions (e.g. iron)

Siderophores (S)
Small molecule secreted by bacteria that bind iron
Measuring bacterial mass in liquid cultures of bacteria
Common methods include:
a) turbidity (the cloudiness of a liquid culture of bacteria –
a measure of total bacteria [live and dead]
b) the number of viable bacteria in a culture –
usually assessed by counting the number of colonies
that grow after streaking a known volume on a plate
Measuring bacterial mass (live + dead) in liquid culture
Measured with spectrophotometer
Measuring viable bacteria
Colony forming units

SUGAR CATABOLISM
• Glycolysis
– Embden Meyerhof Parnas Pathway
– most bacteria
– also animals and plants

STERILIZATION
• All killed
• non-selective
• autoclaving
• 121oC (heat/pressure)
* Heat resistant materials
• ethylene oxide
• Non heat resistant
– usually equipment
• ultra-violet light
– surfaces (e.g operating rooms)
not totally effective
• gamma radiation
– food
– some mail
Disinfection
• Liquids that kill bacteria
– e.g. phenol based
– too toxic for skin surfaces
Antiseptics
• Topical (e.g. skin)
– e.g. iodine or 70% alcohol
– “reduce” bacterial load
ANTIBIOTICS
• Selectively toxic for bacteria
– bactericidal (killing)
– bacteriostatic (growth inhibition)

• no harm to patient
• destroy structures
• present in bacteria
• not present in host

Antibiotics work together
with immune system
Minimal inhibitory concentration
• lowest level stopping growth

• e. g. zone of inhibition around a disk impregnated with antibiotic

• Antibiotics that inhibit cell wall
biosynthesis are bactericidal

• Without cell wall, osmotic pressure
causes bacteria to burst

Antibiotics: Protein Synthesis, Nucleic Acid Synthesis and Metabolism
Principles and Definitions
• Selectivity
– Selectivty8 toxicity9
• Therapeutic index
– Toxic dose/ Effective dose
• Categories of antibiotics
– Bactericidal
• Usually antibiotic of choice
– Bacteriostatic
• Duration of treatment sufficient for host defenses
• Categories of antibiotics
– Use of bacteriostatic vs bactericidal antibiotic
• Therapeutic index better for bacteriostatic antibiotic
• Resistance to bactericidal antibiotic
• Protein toxin mediates disease – use bacteriostatic protein synthesis inhibitor
• Antibiotic susceptibility testing (in vitro)
– Minimum inhibitory concentration (MIC)
• Lowest concentration that results in inhibition of visible growth
– Minimum bactericidal concentration (MBC)
• Lowest concentration that kills 99.9% of the original inoculum
• Combination therapy
– Prevent emergence of resistant strains
– Temporary treatment until diagnosis is made
– Antibiotic synergism
• Penicillins and aminoglycosides
• CAUTION: Antibiotic antagonism
• Penicillins and bacteriostatic antibiotics

Antibiotics that Inhibit Protein Synthesis
Protein Synthesis Inhibitors
• Mostly bacteriostatic
• Selectivity due to differences in prokaryotic and eukaryotic ribosomes
• Some toxicity - eukaryotic 70S ribosomes
Inhibitors of Nucleic Acid Synthesis
• Rifampin, Rifamycin, Rifampicin, Rifabutin (bactericidal
• Quinolones (bactericidal)
nalidixic acid, ciprofloxacin, ofloxacin, norfloxacin, levofloxacin, lomefloxacin, sparfloxacin
Antimetabolite Antimicrobials
• Inhibitors of Folic Acid Synthesis

• Sulfonamides, Sulfones (bacteriostatic)
• Trimethoprim, Methotrexate, Pyrimethamine (bacteriostatic)
Antimicrobial Drug Resistance
Principles and Definitions
• Clinical resistance
• Resistance can arise by mutation or by gene transfer (e.g. acquisition of a plasmid)
• Resistance provides a selective advantage
• Resistance can result from single or multiple steps
• Cross resistance vs multiple resistance
– Cross resistance -- Single mechanism-- closely related antibiotics
– Multiple resistance -- Multiple mechanisms -- unrelated antibiotics
Antimicrobial Drug Resistance Mechanisms
• Altered permeability
– Altered influx
• Gram negative bacteria
– Altered efflux
• tetracycline
• Inactivation
– $-lactamse
– Chloramphenicol acetyl transferase
• Altered target site
– Penicillin binding proteins (penicillins)
– RNA polymerase (rifampin)
– 30S ribosome (streptomycin)
• Replacement of a sensitive pathway
– Acquisition of a resistant enzyme (sulfonamides, trimethoprim)
Pathogenicity
• virulence factors
• number of initial organisms
• immune status
Koch's postulates
• isolated
– diseased not healthy people
• growth
– pure culture
• induce disease
– susceptible animals
• re-isolated
– susceptible animals

Opportunistic infections
• compromised people
– normal flora
– environment

Opportunists - normal flora
• Skin
– Staphylococcus aureus,
– S. epidermidis
– Propionibacterium acnes
• Intestine
– Bacteroides
* high numbers
– Enterobacteriaceae
* low number
Opportunists - environment
» air
• water
• soil
• food
• Opportunists in hospital- nosocomial

Transmission
• airborne droplets
• food
• water
• sexual contact
Host defenses
• Gut
– peristalsis
– defecation
• respiratory tract
– ciliary action
– coughing
– sneezing
• urogenital tract
– urination
COMMENSALS CAUSE DISEASE
WHEN HOSTS DEFENCES ARE LOW
PATHOGENS POSSESS VIRULENCE FACTORS
THAT ENABLE THEM TO CAUSE DISEASE IN
THE PRESENCE OF NORMAL DEFENCES
DETERMINANTS OF BACTERIAL PATHOGENISIS
TRANSMISSION
INFECTING DOSE-INOCULUM
PORTAL OF ENTRY
BACTERIAL VIRULENCE FACTORS
CAPSULES
INVASIVENESS
ADHESINS
EXOENZYMES
TOXINS
CAPSULES
LOCATED EXTERNAL TO THE CELLWALL
COMMON VIRULENCE FACTOR
POLYSACCHARIDES
AVOID OR SURVIVE PHAGOCYTOSIS
ADHESINS
ALLOW BACTERIA TO STICK ON MUCOSAL SURFACE
ADHESINS ARE SURFACE FACTORS
PILI / FIMBRIAE
LPS LIPOPOLYSACCARIDE SIDECHAINS
M PROTEIN
INVASIVENESS
ABILITY TO INVADE HOST CELL
MULTIFACTORIAL COMPLEX PROCESS
MAY INCLUDE ADHESION AND ENZYMES FACTORS

EXOENZYMES
PRODUCE AND SECRETED BY BACTERIA
ENZYMES THAT BREAKDOWN COLLAGEN AND FIBRIN
COLLAGENASES / HYALURONIDASES / FIBRINOLYSINS
ENZYMES THAT BREAKDOWN CELLULAR MATERIALS
PROTEASES / LECITHINASES
ENZYMES THAT DEACTIVATE AND MODIFY ANTIBIOTICS
BETA LACTAMASE
ENZYMES THAT DESTROY NEUTROPHILS
AND MACROPHAGES
LEUKOCIDINE
ENZYMES THAT ACCELERATE FIBRIN CLOT
COAGULASE
TOXINS
2 CLASSIFICATIONS
EXOTOXINS – PROTEINS PRODUCED AND
SECRETED BY BACTERIA
ENDOTOXINS – PART OF THE BACTERIA ITSELF
EXOTOXIN
NEUROTOXINS- AFFECT NERVOUS TISSUE
TETANUS TOXIN
ENTEROTOXINS – AFFECT GASTROINTESTINAL TRACT
CHOLERA TOXIN
CYTOTOXINS – AFFECT CELLS OF VARIOUS TISSUES
DIPHTERIA TOXIN
ENDOTOXINS
ALL GM NEGATIVE BATERIA HAVE ENDOTOXINS
IN OUTER MEMBRANE
RELEASED AS BACTERIA ARE LYSED
RESPONSIBLE FOR SEPSIS AND
SEPTIC SHOCK - FATAL

ectron transport chain of proteins

synthesis of ATP is a series of reduction-oxidation(redox) reaction..
watch and learn by reviewing the questions

lecture slides on renal physio

please check on june 2009 posting

incentive spirotmetry

please check November 2008 posting regarding the use of incentive spirometer
ready: inhale, blow till your dizzy

nervous regulation of arterial pressure

Read chapter 18 Guyton
Learn how the sympathetic system is able to regulate arterial pressure and how the CNS is able to have an overall control on this
Study the reflexes that enable the body to maintain normal arterial pressure in different situations

http://health.howstuffworks.com/adam-200079.htm

http://www.1on1health.com/web/info/hypertension/english/high-blood-pressure-animation/AnimationPage/LookListenLearnType=1

lecture slides on general pathology

please check slides on January 08 posting

A DISASTER WORST THAN ONDOY

GARCIA TOPS the finals

general scores are disappointing. some options are still available

attention raster: get in touch after you and your classmates reach a consensus

CARDIAC CYCLE self-help

helpful links and take the quiz!
blausfuss multimedia
cardiac cycle tutorial
phases of carciac cycle

copy-paste this link to your add bar if links above fail to connect
http://highered.mcgraw-hill.com/sites/0072507470/student_view0/chapter20/animation__the_cardiac_cycle__quiz_1_.html

HERNANDEZ Tops physiolab midterm

followed by
BACTOL
NO NAME
BION SAPALARAN

puppy of kobe my g.dane

a blue-eyed harlequin dane..there were actually 12 puppies but only 2 managed to survive..this is my puppy share

TURNER tops physiolab exam

followed by GAYOLES and BACTOL

BACTOL AND GAYOLES top-notch in physio lec exam

regenerative medicine

an exciting and rapidly rising new field of medicine dedicated to using stem cells to repair and replace damaged cells and tissues. While research continue to move forward some centers(mentioned in previous article) are already using stem cells to treat heart diseases, nervous system dysfunction and malignancies. The possibilities seemed limitless. This is science and technology enabling extra lease on life. Amazing!

http://stemcells.nih.gov/info/scireport/2006report.htm
ohri.ca/programs/regenartive

ms Sapalaran tops physio practicals

autologous adult stem cell transplant

using one's own cell scientists can convert these cells into stem cells and using growth factors 'educate' these cells to target specific damaged tissues. once grafted themselves in these areas of tissues or organs regeneration and repair begins. hundreds of cardiac patients has undergone this treatment and results are quite encouraging. soon they may also be able to grow organs for transplant from stem cells in the laboratory. either way future is limitless for stem cell therapy..

reference

transplant organs from stem cell

regenocyte therapy

Here are the top eight stem cell treatment centers in the world. There are two in Latin America, two in Europe, one in Israel, and three in Asia. Why are they "top?" Because they are led by top-notch physicians who are also outstanding stem cell researchers, including world #1s in stem cells:


for Cancer & Leukemia (Israel),
for Congestive Heart Failure (Thailand),
for Diabetes (Argentina),
for Kidney (Dominican Republic),
for MS (China & Israel),
for Optic Nerve Disorders (China),
for Parkinson's (Germany)**,
and the unquestioned world pioneer in "Complete-break Spinal Cord Injury" (Portugal).

practicals in lab tomorrow

please review the histology tutorial...

smooth muscle tutorial

whfreeman.com

gone too soon

rest in peace mj....
michael is finally back...see last rehearsal 2 days before he left

http://www.youtube.com/watch?v=FcCL8vZNSe0

physiology of muscle contraction

be sure to digest everything that is explained and take the quiz. capy paste if the link won't work
have fun


http://www.getbodysmart.com/ap/muscletissue/contraction/propagation/tutorial.html
www.getbodysmart.com
www.blackwellpublishing.com

membrane potential tutorial

whfreeman.com membrane potential

renal physiology lec slides

1.maintenance of the body fluid
compositions and volumes

2.production of a
low-volume, highly concentrated urine to rid the body of metabolites,
drugs, and other undesirable substances without wasting water
Distribution of Water among the Body Fluids
 body typically contains about 60% water by weight (1 L H2O = 1 Kg)
 intracellular fluid (67% inside cells) and extracellular fluid (33% outside
 cells)
 plasma water (25%) or
 interstitial fluid (75%)
Shifts of Water between Body Fluid Compartments
 Osmotic gradients

 asymmetric distribution of ions across a semi-permeable membrane

 Water will continue to traverse the cell membrane until the
 osmotic pressure on each side of the membrane becomes the same
 (equilibration)
FUNCTIONS:
1. Blood volume and composition
2. Blood pressure
3. Metabolism
PRIMARY FUNCTION…
EXTERNAL ANATOMY
A. Hilus
B. Layers of the Kidney
a. renal capsule
b. adipose capsule
c. renal fascia
NEPHRON
- functional unit of the kidney

3 basic functions:
A. filtration
B. secretion
C. reabsorption

Parts:
A. Renal Corpuscle
B. Renal Tubule
RENAL CORPUSCLE
A. Glomerulus
B. Glomerular (Bowman’s) Capsule

Parts of the renal corpuscle….

The Renal Corpuscle…. Convoluted tubules…

CORTICAL AND JUXTAMEDULLARY NEPHRONS
- Loop of Henle
- Location of Glomerulus
Functions of the Nephrons:
1. Control blood concentration and volume
2. Regulate blood pH
3. remove toxic wastes from the blood

Processes of Urine Formation:
A. Filtration
B. Reabsorption
C. Secretion
GLOMERULAR FILTRATION
- principle is forcing of fluids through a membrane
- occurs in the renal corpuscle
- BP forces water
- resulting fluid is called the FILTRATE
- most proteins are large enough to pass through the endothelial-capsular membrane

 Approximately 25% of the cardiac output or 1200 ml of blood per minute is received by the kidneys.

 One liter of urine is the end product of more than 1000 liters of circulating blood processed through the kidneys.
 The JGA plays a major role in the renin-angiotensin-aldosterone system
 The JGA has also been implicated in the autoregulation of GFR.
renin-angiotensin system
 or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that helps regulate

 long-term blood pressure
 and blood volume in the body.
 The system can be activated when there is a loss of

 blood volume or
 a drop in blood pressure
 decreased perfusion of the juxtaglomerular apparatus in the kidneys then the juxtaglomerular cells release the enzyme renin.

 Renin cleaves an inactive peptide called angiotensinogen, converting it into angiotensin I.

 Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE), which is found mainly in lung capillaries
 it is a potent vasoconstrictor.

 In the kidneys, it constricts glomerular arterioles

 increases the arterioler resistance, raising systemic arterial blood pressure

 In the adrenal cortex, it acts to cause the release of aldosterone
 Aldosterone acts on the tubules
 ---reabsorb more sodium and water from the urine.

 acts on the central nervous system to increase a person's appetite for salt, and to make them feel thirsty.
Clinical significance
 The renin-angiotensin system is often manipulated clinically to treat high blood pressure.

 Inhibitors of angiotensin-converting enzyme (ACE inhibitors) are often used to reduce the formation of the more potent angiotensin II.

 angiotensin receptor blockers (ARBs) can be used to prevent angiotensin II from acting on angiotensin receptors.

 180 L/day > amount of filtrate that enters the capsular space

 178-179 liters are returned to the bloodstream by reabsorption

 1-2 liters are excreted as urine

Special features of the renal corpuscles enhance their blood filtering capacity:
1. Glomerular capillaries are long
2. The filter (endothelial-capsular membrane) is porous and thin
- fenestrations generally do not restrict
passage of solutes
3. Capillary blood pressure is high
Net Filtration Pressure
Three Main Pressures in the glomerulus:
A. GLOMERULAR BLOOD HYDROSTATIC PRESSURE (GBHP)
- blood pressure inside the glomerular capillaries
- usually 60 mmHg

B. CAPSULAR HYDROSTATIC PRESSURE (CHP)
- due to: a. walls of the capsule
b. fluid that has already filled the renal tubule
- filtrate push back
- 15 mmHg amount of push

C. BLOOD COLLOID OSMOTIC PRESSURE (BCOP)
- due to the presence of PROTEINS
- the greater the solute concentration, the greater is its osmotic
pressure
- usually 27 mmHg
NFP = GBHP - (CHP + BCOP)
Promotes Oppose
Filtration Filtration

Calculation:

GUYTON: GBHP = 60 mmHg
BCOP = 32 mmHg
CHP = 18 mmHg
GLOMERULAR FILTRATION RATE
- the amount of filtrate in all renal corpuscles of both kidneys every minute
- in normal adults ------ 125 ml / min ; 180
L / day
- directly related to NFP
Regulation of GFR
systemic blood pressure and
diameter of afferent and
efferent arterioles
Principal mechanism:
A. Renal Autoregulation of GFR
- operates by negative feedback system
- involves the juxtaglomerular apparatus
B. Hormonal Regulation
Two hormones:
A. Angiotensin II
> Stimuli for renin secretion
1. decreased delivery of fluid and NaCl
to the macula densa
2. decreased stretch of the juxtaglomerular cells
3. sympathetic nerve stimulation

Important action of ANGIOTENSIN II:

1. Vasoconstriction
2. Aldosterone (adrenal cortex)
3. Thirst (hypothalamus)
4. ADH (posterior pituitary gland)
B. Atrial Natriuretic Peptide (ANP)
- secreted by cells in the atria
- stretch of the heart

Important action:
1. promotes excretion of both water and sodium
2. increases GFR > increasing the permeability of
the filter
> dilating the afferent arteriole
3. lowers blood pressure
4. reduces water retention
C. Neural Regulation
- sympathetic stimulation - vasoconstriction
TUBULAR REABSORPTION
1. REABSORPTION IN THE PCT
A. Sodium
- concentration of Na inside tubule cells are low
- interior of the cell is negatively charged
- passive diffusion of Na+ through leakage channels
- Na pumps expel Na through primary active transport
- K+ can diffuse back out through K+ leakage channels
-
MAIN EFFECT: reabsorption of Na+
- active transport of Na+ promotes reabsorption of water through osmosis
- reabsorption of Na+ increases osmotic pressure in the tubule cytosol and in the blood in the peritubular capillaries
B. Nutrients
- 100% of filtered glucose, amino acids and other useful metabolites are reabsorbed in the PCT
- reabsorption by Na+ symporters (secondary active transport)
- Na+ symporter (integral membrane protein)
- substances brought into to the PCT by SYMPORTERS generally leave by facilitated diffusion

Values:
100% - nutrients
80 to 90% - HCO3
65% - Na+ and water
50% - Cl+ and K+
2. REABSORPTION IN THE LOOP OF HENLE
- cells in the thick ascending limb of the Loop of Henle features SYMPORTERS
- simultaneously reclaim one Na+, one K+ and two Cl+ from the filtrate
- secondary active active transport mechanism
- K+ are allowed to recycle through leakage channels
-
MAIN EFFECT: reabsorption of Na+ and Cl+
- DESCENDING LIMB – absorbs water
- ASCENDING LIMB – little or no water

3. REABSORPTION IN THE DCT AND COLLECTING DUCTS
- fine tuning of salt and water reabsorption
- two hormones act on PRINCIPAL CELLS – regulate
absorption

A. Aldosterone
- secreted by adrenal cortex
- increases Na+ and water reabsorption by principal
cells

B. Antidiuretic Hormone (ADH)
- secreted by the post. pituitary gland (hypothalamus)
- increases water permeability by the principal cells
low water concentration in the blood


increased secretion on ADH (osmoreceptors in the hypothalamus


stimulate production of water channels


increased permeability of the apical membranes of principal cells


water is passes into the cells and into the blood

NOTE:
Absent ADH - 20 liters/day of dilute urine
ADH present - 400-500 ml/day of concentrated urine
TUBULAR SECRETION
SECRETION OF H+
- normal blood Ph (7.35 to 7.45)
- occurs in the epithelial cells of the PCT and collecting ducts

Ways in which the cells in the renal tubule can raise the blood pH:
1. secreting hydrogen ions into the filtrate
2. reabsorbing filtered HCO3 (important buffer of H+)
3. producing new HCO3 to augment buffering of H+
CO2
Diffusion from tubular blood
Diffusion from tubular fluid
Metabolic reactions within epithelial cells


presence of carbonic anhydrase (CA)


CO2 combines with water


Forming carbonic acid H2CO3
H2CO3 dissociates into


H+ and HCO3 ions


H+ is secreted into the tubular fluid (filtrate)
accomplished by Na+/H+ antiporters


HCO3 diffuses into the peritubular capillaries
NOTE: for every H+ secreted, one ion of HCO3 is returned to the blood….
secreted H+


combines with filtered HCO3


forming H2CO3


dissociates into CO2 and H2O


CO2 diffuses into the tubule cells


CO2 joins with water forming H2CO3
NOTE: as the H+ is secreted into the tubular fluid, HCO3 is reabsorbed into the blood together with Na+

OVERALL RESULT: reabsorption of Na+ and HCO3
Tubular reabsorption (movement from tubule into interstitial fluid and then blood)
 A) Proximal convoluted tubule -most reabsorption of substances occurs here
 Sodium ions reabsorbed via active symporter pumps.
all glucose and amino acids move with Na in symporter pumps.
 most Cl– and almost all HCO3- ions passively diffuse down their electrical gradient, following Na+
 positive ions (K+ and Ca++) diffuse down their electrical gradient, following negatively charged HC03 and Cl-
 most water moves to accumulation of ions in interstitial fluid (movement of Na+, Cl– and other dissolved substance) by osmosis (osmotic pressure being higher in interstitial fluid than filtrate)
 B). Descending loop of Henle (always permeable to H2O)
 passive H2O reabsorption following osmotic gradient set up by Na and CL reabsorption by ascending loop in medulla (and accumulation of urea also in medulla)
 C. Ascending loop of Henle (always impermeable to H2O)
 does not allow water back into filtrate but pumps out Na and Cl
(Medullary osmotic gradient magnified by this countercurrent multiplier
 D. Distal convoluted tubules
 a) Ca+ reabsorption promoted by PTH.
b) more Cl and Na+ ions reabsorbed promoting little more water reabsorption
 From PCT to DCT all reabsorption is obligatory-it will always occur.

 In the collecting ducts, hormones determine reabsorption.
 E . collecting ducts

 (reabsorption/secretion due to levels of hormone, ADH or Aldosterone)
 water...
a) if high levels of ADH then more water pores made in cells so more water reabsorbed (forming little concentrated urine)
 b) if low levels of ADH then less water pores made in cells so water not reabsorbed (forming copius dilute urine)
 Sodium
 c) if high levels of aldosterone then more Na/K+ pumps made in cells so more Na reabsorption/K secretion
 d) if low levels of aldosterone less Na/K+ pumps made in cells so less Na reabsorption/K secretion.

do you know brownian motion?

diffusion and brownian motion
In cell biology, diffusion is a main form of transport of necessary materials such as amino acids through cell membranes watch this
http://galileoandeinstein.physics.virginia.edu/more_stuff/Applets/brownian/brownian.html

APOPTOSIS- for curious Ms Hernandez

what difference is there between apoptosis and necrosis
Disintegration of cells into membrane-bound particles that are then eliminated by phagocytosis or by shedding.

normal cells commit suicide when they were finished being useful
while cancer cells lived on and on. Now, researchers have found a way to trick cancer cells into bowing out gracefully... cure for cancer?

http://www.whfreeman.com/kuby/content/anm/kb04an01.htm


see the death enzymes- caspases and the sound of dying!!
http://www.youtube.com/watch?v=9KTDz-ZisZ0&feature=related

cell tutorial

http://www.tvdsb.on.ca/westmin/science/sbi3a1/Cells/cellquiz.htm --'copy-paste' this link to your address bar



http://www.wiley.com/legacy/college/boyer/0470003790/animations/cell_structure/cell_structure.htm

study of cell - tutorial

http://www.biology.arizona.edu/DEFAULT.html -- copy paste this link in your address bar

GAITANO, QUERUBIN- top micropath-lec finals

LIM, PARK - top physiolab finals

surging above the rest in physio-lec finals
OGACION CORREOS PARK QUEROBIN DEOCAMPO ALAVE ACLAO

in micropath lab
TIONKO LASTIERRI BLASURCA LABARO OCACION

on caloric restriction, exercise and longevity

Caloric restriction (CR) refers to a dietary regimen low in calories without undernutrition. This regimen seemed to delay the onset of various chronic disorders thus increasing longevity. Some people might find this program starving and results in low quality of life.

So instead of having huge reduction of caloric intake another option is to increase caloric expenditure by exercise. Though some studies on this showed conflicting results.

But if you are really the lazy-kind and hate exercise and being starved close-to-death there is one thing left for you to do. Take resveratrol(longevity pill?). It goes directly to the triggering mechanism that prevents dna damage due to extraneous factors and thus delay onset of inflammatory and maybe neoplastic conditions : activating the sir2 genes known as longevity genes.

http://genesdev.cshlp.org/content/17/3/313.full
http://www.sciencedaily.com/releases/2008/05/080514064921.htm
http://blog.wired.com/wiredscience/2008/07/caloric-restric.html

"Nothing in this world can take the place of persistence. Talent will not; nothing is more common than unsuccessful people with talent. Genius will not; unrewarded genius is almost a proverb. Education will not; the world is full of educated derelicts. Persistence and determination alone are omnipotent. The slogan "press on" has solved and always will solve the problems of the human race”

--so press it on guys

HIV

human immunovirus penetrating T-cell and penetrate deep into the nucleus to insert its genetic material into host's genome for reproduction. When it matures or goes out again to infect other cells thus disrupting the immune function of lymphocytes.

check slides for common viral infection in january 08 posting.

menstrual cycle tutorial

follow these links

monthly cycle

http://health.howstuffworks.com/menstruation.htm


http://msnbcmedia.msn.com/i/msnbc/Components/Interactives/Health/WomensHealth/zFlashAssets/menstrual_cycle_dw2%5B1%5D.swf

spermatogenesis and oogenesis
http://wps.aw.com/bc_martini_eap_4/40/10469/2680298.cw/content/index.html

gi lecslides

GASTROINTESTINAL PHYSIOLOGY
GENERAL PRINCIPLES OF GASTROINTESTINAL FUNCTION
-motility, nervous control and blood circulation

TRANSPORT AND MIXING OF FOOD IN THE ALIMENTARYTRACT

SECRETORY FUNCTION OF ALIMENTARY TRACT

DIGESTION AND ABSORPTION

PHYSIOLOGY OF GI DISORDER
GENERAL PRINCIPLES OF GI FUNCTION
 GIT PROVIDES – water, elctrolytes and nutrients


 Requirements
1. movement of food thru GIT
2. secretion digestive juices and digestion of food
3. absorption of digestive products
4. circulation of blood thru GIT
5. control of all functions by nervous/hormonal system
 TYPICAL INTESTINAL WALL
1. serosa
2. longitudinal muscle layer
3. circular muscle layer
4. submucosa
5. mucosa

THE GIT SMOOTH MUSCLE
 Function as a syncytium – when action potential is elicited anywhere within the muscle mass it travels in all directions in the muscle

 electrical activity – 2 basic types
 1. slow waves – not action potentials
 - slow undulating change in membrane potential
 - undulating activity of sodium potassium pump
 - control the appearance of spike potentials
 2. spike potential – true action potentials
 - occurs when membrane potentials is 40millivolt more
 positive
 Factors that depolarize the mambrane
 1. stretching of the muscle
 2. stimulation by acetylcholine
 3. stimulation by parasympathetic nerves secreting aceytylcholine
 4. stimulation by specific GIT hormones

 Factors that make the membrane more negative
 1. effect of norepinephrine or epinephrine
 2.stimulation of sympathetic nerves secreting norepinephrine
CALCIUM IONS AND MUSCLE CONTRACTION
 Muscle contraction occurs in response to entry of calcium ions
in muscle fibers

In slow waves calcium ions do not enter the membrane but instead only sodium ions thus no contraction occur


causes of tonic contraction of GIT smooth muscle
1. repetitive series of spike potentials
2. hormones
3. continuous entry of calcium ions

 ENTERIC NERVOUS SYSTEM
1. myenteric plexus or aurbach’s plexus
- between longitudinal and circular muscular layers
- controls GIT movement
2. submucosal or Meissner’s plexus
- located in the mucosa
- control secretion and local blood flow
AUTONOMIC CONTROL OF GIT
 Parasympathetic innervation – cranial and sacral divisions
- cranial part-transmitted almost entirely by vagus nerve
- covers esophagus, stomach, pancreas, first part of large intestine
- sacral part originates from 2nd 3rd 4th segment of spinal cord pass
thru pelvic nerves – distal large intestine

 Sympathetic innervation
- originate between T5 and L2
- from cord enter the sympathetic ganglia and pass thru celiac ganglion
- generally inhibitory effect on GIT
 Many afferent nerve fibers arise in the gut
 Some may have their cell bodies in the enteric nervous
system itself

 These nerves can be stimulated by
1. irritation of the gut mucosa
2. excessive distention of the gut
3. specific chemical substances in the gut

 Signals transmitted thru these may cause excitation or
inhibition
THE GIT REFLEXES
 The anatomical arrangement of the enteric nervous system
and its connection to the sympathetic and parasympathetic
nervous systems support 3 types of GIT reflexes

1. reflexes that occur entirely wihtin the enteric nervous system
- control of GI secretion, peristalsis, mixing contraction

2. reflexes from the gut to the prevertebral sympathetic ganglia then
back to the GIT
- gatrocolic reflex, enterogastric reflex,colonoileal reflex

3. reflexes from the gut to the spinal cord or brainstem and then back
to the GIT
- pain inhibition, defecation reflex,
HORMONAL CONTROL OF GIT MOTILITY
 Cholecystokinin – from the jejunum in response to the presence of
fatty substance in the intestinal contents
- increase contractility of gallbladder
- slows stomach emptying

 Secretin – from doudenum in response to acidic gastric juice
- mild inhibitory effect on motility of GIT

 Gastric inhibitory peptide – from upper small intestine in response to
fat and carbohydrate
- slows gastric emptying
FUNCTIONAL TYPES OF MOVEMENTS IN THE GIT
 Two basic types of movements

1. propulsive - move cause food to move forward
- peristalsis- contractile ring appears around the . gut and then moves forward
- usual stimulus is distention
- function of myenteric plexus
- peristaltic reflex or law of the gut

. mixing movements – peristaltic contraction can cause mixing contractions if forward movement of the intestinal is blocked by a sphincter

- local constrictive rings occur at regular interval-
relaxes- reappear at other points- chopping effect


 Splanchnic circulation- blood flow thru the alimentary tract, spleen
pancreas and liver

 Anatomy of GI blood supply- superior mesenteric artery
- inferior mesenteric artery
- supply small and large intestine
-enters the wall by circling in both directions around the gut
- penetrates into the wall and spread along
1. villi
2. muscle bundles
3.submucosal vessels beneath the epithelium
EFFCT OF GUT ACTIVITY AND METABOLIC FACTORS ON GI BLOOD FLOW
 Under normal conditions GI blood flow is directly related to
level of local activity

 After a meal the motor, secretory,absorptive activities all increase- blood flow likewise increases by 100-150%

 Possible causes of increased blood flow
1.release of vasodilator substances:
cholecystokinin,vasoactive intestinal peptides,gastrin,secretin
2. release of kallidin and bradykinin by gastrointestinal glands
3.decrease in O2 concentration
COUNTERCURRENT BLOOD FLOW MECHANISM IN THE VILLI
 Opposite direction of arterial flow into the villi and venous flow out of the villi

 Blood O2 diffuses out of the arterioles directly into the venules without being carried to the tip of the villi

 Shunting of blood in disease condition can cause ischemia
or disintegration of villus
NERVOUS CONTROL OF GIT BLOOD FLOW
 Stimulation of parasympathetic nerves increase blood flow

 Stimulation of sympathetic nerves cause vasoconstriction-
last for few minutes because of autoregulatory escape

 Major value of sympathetic vasoconstriction is the shutting
off of GI blood flow to the brain and heart during exercise
and shock

CHEWING REFLEX
 Presence of food in the mouth reflex inhibition of muscle of mastication dropping of lower jaw
stretch reflex of jaw muscles rebound contraction
raises the jaw that cause closure of the teeth
compresses the food again
SWALLOWING
1.voluntary stage
 – food is voluntarily rolled into posterior pharynx by action of tongue

- hence the process becomes almost entirely automatic

2. pharyngeal stage
 – receptors around the pharynx(tonsils) send impulses to the brainstem initiating as series of pharyngeal muscular contractions

a soft palate is pulled upwards to close the post. nares
b. palatopharyngeal folds are pulled medially
c. vocal cords of the larynx are approximated, pull of larynx
upwards and anteriorly
d. enlarging of the pharyngeal opening,relaxation of upper
esophageal sphincter
e. contraction of esophageal muscle

 Entire process occurs in 1 to 2 seconds

NERVOUS CONTROL OF THE PHARYNGEAL STAGE OF SWALLOWING
 Tonsillar pillars – most sensitive tactile area of the pharynx
- impulses from this area are transmitted to trigeminal and glossopharyngeal nerves into medulla oblongata—deglutition center

motor impulses from the swallowing center to the pharynx
and esophagus are transmitted by 5th, 9th,10th and 12th cn

 Pharyngeal stage of swallowing is a reflex act
1 – 2 seconds in duration, interrupting respiration for only a fraction
of a second
3. ESOPHAGEAL STAGE OF SWALLOWING
 Esophagus has 2 types of peristalsis:

1.primary peristalsis – continuation of pharyngeal peristalsis

2. secondary peristalsis – carries food left behind by primary
peristalsis to distal esophagus
- initiated partly by intrinsic neural circuit

Function of lower esophageal sphincter – thickening of circular
muscle in GE junction
- prevents reflux of acidic gastric juice
MOTOR FUNCTION OF THE STOMACH
 1. storage of large quantities of food – vagal reflex can reduce
muscle tone of the stomach for accomodation- 1.5 liters

2. mixing of food with gastric juice – chyme

3. slow emptying into the small intestine – intensity of antral
contraction determines the rate of gastric emptying
- role of pylorus- contracted almost at all times

 Hunger contractions – strong tetanic contractions of the body of the
stomach when it is empty for sometime
REGULATION OF STOMACH EMPTYING
Regulated by signals coming from the
stomach and duodenum


Stomach signals are
1. nervous signals caused by distention of the stomach
2. hormone gastrin released from antral mucosa

- both increase pyloric pumping force
- promote gastric emptying

Duodenal signals
- could also be nervous and hormone
- depress pyloric pumping
- increase pyloric tone

GASTRIC FACTORS THAT PROMOTE EMPTYING
 Increased food volume in the stomach increased emptying

 Gastrin from antral mucosa – potent effect on secretion of acid
-enhance pyloric pumping

 Duodenal factors that inhibit emptying
- inhibitory effect of enterogastric nervous reflex –

GASTRIC FACTORS THAT PROMOTE EMPTYING
 Factors that excite

1.degree of distention of duodenum
2. degree of irritation of duodenal mucosa
3. degree of acidity of duodenal chyme
4. degree of osmolality of chyme
5. presence of breakdown products
HORMONAL FEEDBACK FROM THE DUODENUM IN INHIBITING GASTRIC EMPTYING
 Not only nervous reflex from duodenum inhibits gastric emptying hormones from duodenum do as well

 Stimulus for secretion of these hormone is mainly FAT

HORMONAL FEEDBACK FROM THE DUODENUM IN INHIBITING GASTRIC EMPTYING
1. cholecystokinin – from jejunal mucosa
2. secretin – from duodenal mucosa
3. gastric inhibitory peptide
- inhibit pyloric pump activity
- increase the strength of pyloric sphincter contraction
MOVEMENTS OF THE SMALL INTESTINE

 As with elsewhere in the GIT – mixing and propulsive

 Mixing contraction(segmentation contractions)
- distention with chyme stretch of intstinal wall concentric
contraction spaced at interval
propulsive contraction
- contractile ring appears then moves forward squeezing contents
towards the ileocecal sphincter

Function of ileocecal valve – prevent back flow of fecal content to the small intestine

MOVEMENTS OF THE COLON
 Principal functions
 1. absorption of water and elctrolytes
 2.storage of fecal matter

 Mixing movements and propulsive movements
 Mass movement - a modified type of peristalsis – constrictive ring
occurs at area of distention then rapidly 20 cm of colon distal
to this point contract as a unit forcing fecal material en mass
down the colon
Initiation of mass movemenet – gastrocolic and duodenocolic
reflexes
MOVEMENTS OF THE COLON
 Mixing movements and propulsive movements

Mass movement
 - a modified type of peristalsis – constrictive ring occurs at area of distention then rapidly 20 cm of colon distal to this point contract as a unit forcing fecal material en mass
down the colon
Initiation of mass movement
gastrocolic and duodenocolic reflexes

 Rectum is empty most of the time
 Reasons - presence of weak sphincter at the junction
between sigmoid and rectum
- sharp angulation also at the same area

Dribbling of fecal matter to the anus is prevented tonic constriction of 1. internal anal sphincter
2. external anal sphincter

DEFECATION REFLEXES
 Feces enter the rectum distention of rectal wall
initiate afferent signals myenteric plexus
peristaltic waves descending colon, sigmoid and rectum
forcing feces toward the anus
SECRETORY FUNCTIONS OF GIT
 Primary functions 1. secretion of digestive enzymes
2. secretion of mucus – lubrication and
protection

 Anatomical types of glands
1. single cell mucus glands
2. crypts of lieberkuhn- pits- invaginated epithelium
3. tubular glands – in stomach and duodenum
4. complex glands- salivary, pancreas, liver

BASIC MECHANISMS OF STIMULATION OF THE GIT GLANDS
 EFFECT OF LOCAL CONTACT AND ENTERIC NERVOUS STIMULI
-types of stimuli 1. tactile
2. chemical irritation
3. distention of gut wall

 Parasympathetic stimulation – increase secretion
 Sympathetic stimulation – increase/decrease secretion
 Regulation of secretion by hormones
DAILY SECRETION OF INTESTINAL JUICES
 Saliva 1000
 Gastric secretion 1800
 Pancreatic secretion 1000
 Bile 1000
 Small intestine 1800
 Brunners gland 200
 Large intestine secretion 200
 total 8700
SECRETION OF SALIVA
 Principal glands- parotid, submandibular,sublingual glands
 2 major types of proteins in the saliva
1. serous secretion – ptyalin –enzyme
2. mucous secretion – mucin – lubrication

 Functions of saliva –
1. flow – washes away bacteria
2. contains factors that destroy bacteria
- thiocyanate ions, proteolytic enzyme
GASTRIC SECRETION
 ESOPHAGEAL SECRETION –entirely mucoid for lubrication

 Mucus glands lined the entire surface of the stomach
 2 tubular glands
1.oxyntic(gastric) glands – hcl, pepsinogen, intrinsic fator, mucus
2. pyloric glands – gastrin – mucus, pepsinogen

 Secretions from oxyntic glands
3 different types of cell 1. mucus neck cells – mucus
2.peptic(chief)cells – pepsinogen
3. parietal cells – hcl and intrinsic factor
REGULATION OF GASTRIC SECRETION BY NERVOUS AND HORMONAL MECHANISMS
 Basic neurotransmitters or hormones that stimulate gastric
secretion

1. acetylcholine – stimulates all types glands
2. gastrin- parietal cell- acid
3. histamine- parietal cell- acid

 All function by binding first to the receptor in the secretor cell


REGULATION OF GASTRIC SECRETION BY NERVOUS AND HORMONAL MECHANISMS
 Stimulation of acid secretion

 Nervous stimulation- half of signal for gastric secretion comes from
the brain and other half from local reflexes within the enteric n.s.

-reflexes are stimulated by
1. distention of stomach
2.tactile stimulation of stomach surface
3.chemical stimuli
REGULATION OF ACID SECRETION

 Stimulation of acid secretion by gastrin
- signals from vagus and local reflexes stimulates antral stomach to
secret gastrin from G- cell in the pyloric gland
- gastrin itself can then stimulate parietal cell to strongly secrete hcl


 Role of histamine in controlling gastric secretion
-histamine is continuously produced in gastric mucosa
- by itself it causes little secretion
-in the presence of acetylcholine and gastrin it can enhance acid secretion significantly
PANCREATIC SECRETION
 Pancreas is located parallel and beneath the stomach

 Secretions 1. insulin by islet of Langerhans
2. digestive enzymes – pancreatic acini
3. sodium bicarbonate solution from the ducts

 -- secreted to presence of food or chyme in the
upper small intestine
Digestive enzymes of pancreas
For PROTEIN
trypsin
chemotrypsin
carboxypetidase
For CARBOHYDRATE
amylase
dissacharidases
For FATS
lipase
phospholipase
cholesterol esterase
 Trypsin inhibitor – prevents activation of enzymes inside the
glandular cell


 Bicarbonates – serve to neutralized acid being emptied into
the duodenum

REGULATION OF PANCREATIC SECRETION
 Basic stimuli –
 1.acetylcholine –from parasympathetic
 nerve ending to enteric n.s.

2.gastrin – from stomach

3. CCK – from jejunal and duodenal mucosa

4.secretin – jejunal mucosa

SECRETION OF BILE AND FUNCTION OF BILIARY TREE
 One of the function of the liver- secretion of bile



 1. fat digestion- a. emulsify large fat particles to smaller ones
 b. aid in transport and digestion of fat

 2. excretion of several waste products from blood
 - bile, excess of cholesterol
 - bilirubin, end product of hemoglobin destruction

 PHYSIOLOGIC ANATOMY OF BILIARY SECRETION
bile- secreted by hepatocytes into bile canaliculi bile flows to
bigger ducts- terminal bile ducts reaching hepatic ducts
common bile duct cystic duct gallbladder

 Composition of bile 1. bile salts – from cholesterol
2. bilirubin
3. cholesterol
4. lecithin

 Emptying of the gallbladder – CCK
 Bile salts – detergent or emulsifying function
--form micelles lipids to facilitate absorption
SECRETIONS OF SMALL INTESTINE
 Brunners gland- mucus gland located in the duodenum
- secretes mucus in response to
1. tactile stimuli
2.vagal stimulation
3. gastrointestinal hormones
- mucus for protection of duodenal wall from gastric juice

crypts of Lieberkuhn – entire surface of small intestine
- secretions by epithelial cells – 1000cc/day
enzymes in the epithelial cells 1. peptidases
2. dissacharidases
3. lipase

SECRETIONS FROM LARGE INTESTINE
 Crypts of Lieberkuhn - secrete mucus
-- no enzymes , no villi
 mucus protects wall against excoriations
--provides an adherent medium for holding fecal material
together
-- protects wall from bacteria

 Secretion of water and electrolytes – in response to irritations to dilute the irritating factors causing raid movement of feces towards anus
DIGESTION AND ABSORPTION IN GIT
 Food on which the body lives: carbohydrates
fats
proteins

-- not absorbed in their natural form
 Hydrolysis– basic process of digestion

 Carbohydrates– large polysaccharides that are made up of
monosaccharide


 -- monosaccharides are bound together by the process condensation

--condensation- one hydrogen ion has been removed from one mono -saccharide and one hydroxyl ion from another

 During digestion one enzyme return the hydrogen and hydroxyl ions back:
resulting in seperation of the polysaccharide to monosccharide

 Triglycerides– consists of free fatty acids condensed with
glycerolmolecules
condensation – 3 molecules of water

digestion- fat enzyme returns the 3molecules of water
(hydrolysis)


 Proteins– formed from amino acids that are bound together by peptide linkages
-- hydroxyl ion is removed from one amino acid
and hydrogen ion from another
-- digestion- reverse effect of hydrolysis
DIGESTION OF CARBOHYDRATES
 3 major sources of carbohydrates:
1. lactose – galactose and glucose
2. sucrose – fructose and glucose
3. starch – polysaccharide
digestion in mouth and stomach
ptyalin
-from saliva– hydrolyze starch into maltose
- amylase is blocked by acid in the stomach

small intestine
amylase
- pancreatic secretion
- starches almost totally converted to maltose
 disacharidases from intestinal epithelial membrane

monosacharides
 Final products of carbohydrate digestion

goes to portal blood
DIGESTION OF PROTEIN
pepsin
-peptic enzyme in the stomach is active in acid
- pepsin digest collagen(collagen tissue component in meat)
-making digestive enzymes able to digest meat

 Digestion by pancreatic secretion
- mostly occuring in the upper small intestine-
duodenum,jejunum
- partially digested protein will be digested by

trypsin
chemotrypsin
carboxypeptidase
Cleaves the a.a. from polypeptide
peptidase
 -digestion of peptides
 -occurs in the epithelial lining of the small intestinal villi
- peptidases protrude thru microvilli of brush border membrane
-final digestion to a.a. occurs in the cytosol of the epithelial cell
- this a.a. then passes to the other side of the membrane and
into the portal blood
DIGESTION OF FATS
triglycerides
 neutral fat that is most abundant in diet

 Phospholipds, cholesterol esters and fatty acid

 Cholesterol – no fatty acid component but with same characteristics with fatty acid

lipase
 Digestion of triglycerides by pancreatic lipase
 Pancreatic lipase is enough to digest all triglycerides
 End product of fat digestion is free fatty acid and
monoglyceride

bile + agitation pancreatic lipase
 Fat emulsified fat free fatty acid
monoglycerides
BASIC PRINCIPLE OF GASTRO INTESTINAL ABSORPTION
 Total quantity that must be absorbed each day is equal to the
 ingested fluid(1.5liters) + GI secretions(7 liters)= 8-9liters
 All but 1.5 is absorbed in the small intestine
 1.5 is pass on to the large intestine
 The absorptive surface of the intestinal mucosa- villi
-valvulae conniventes(folds of kerckring)

basic mechanism of absorption
active transport
diffusion
ABSORPTION IN THE SMALL INTESTINE
 Several hundred gms of carbohydrates

 50-100gm of amino acid

 50- 100 gms of ions

 7-8 liters of water

 Absorption of water
- entirely by diffusion
- when chyme is dilute-water is absorbed thru
intestinal mucosa and into blood supply of villi
by osmosis

-hyperosmolar chyme-water is transferred to the lumen to make it isosmotic with plasma

ABSORPTION OF IONS
 Active transport of sodium
 30 gms secreted into the lumen each day
 5 – 8 gms from diet
 Total of 25 – 35 gms absorbed each day
 Absorption of chloride ions – follow the electrogradient created by
sodium absorption
 Absorption of bicarbonate –large quantities must be reabsorbed form pancreatic secretion
-sodium absorption results in excretion of hydrogen ion- bicarbonate would combine with this forming carbonic acid CO2 and H2O. Water remains with chyme but CO2 is reabsorbed

ABSORPTION OF NUTRIENTS
 Absorption of carbohydrates
- all in the monosaccharide form
- absorbed thru the cell membrane by active
transport
- selective
- sodium co-transport for glucose and galactose
 Absorption of protein
- absorbed in the form of dipeptides,
tripeptides, amino acid

- needs transport protein thus facilitated diffusion
- some thru sodium co-transport

 Absorption of fat
-dissolved in the central liquid portion of a miscelle -ferried t owards brush border diffuse inside the epithelial cell
endoplasmic reticulum triglyceride – chylomicron central lacteal

ABSORPTION IN THE LARGE INTESTINE
 Formation of feces
1000- 1500 cc of chyme pass thru ilececal valve each day
- water and electrolytes are absorbed, <100 cc is left in
in the feces
- absorption – proximal half of the colon
- storage – distal half of the colon

 Bacteria in the colon
- numerous colon bacilli- digestion of cellulose
- substances formed by bacterial activity- vit K, B12,
thiamin and gases
 Composition of feces
-3/4 water and ¼ solid matter
- 30% dead bacteria
30% roughage
- 10-20% fat
-10-20% inorganic matter
- 2-3% protein

PHYSIOLOGY OF GASTROINTESTINAL DISORDER
Disorder of swallowing and esophagus

-paralysis of 5,9 and 10th cranial nerves

-diseases like poliomyelitis or encephalitis-destroy
swallowing center in the brain

-muscle dystrophy – destroy swallowing muscles

-myasthenia gravis or botulism – failure of neurotrans
mission
 Abnormalities
1. complete failure of swallowing
mechanism
2. failure of glottis to close
3. failure of soft pallate to close

 Anesthetic patients--

ACHALASIA
 Lower esophageal sphincter fails to relax thus food
fail to pass to the stomach
 Pathology is nonfunctioning of myenteric plexus in
the lower third of the esophagus

 Esophageal stasis
 Substernal pain- rupture causing death
 Treatment – esophageal baloon
- antispasmodic drugs
DISORDER OF THE STOMACH
 Gastritis – inflammation of gastric mucosa
- very common
- superficial-not very harmful but deep
involvement can lead to complete atrophy
- acute severe form- ulcerative excoriations
- cause is unknown
- mostly due to foods that are damaging to
mucosal barrier –alcohol and aspirin

 Gastric barrier and its penetration in gastritis
- gastric mucosal barrier -cause of poor absorption
in the stomach
1. mucus cell secreting viscid and adherent mucus
2. tight junction between cells

 Gastric barrier becomes inflammed in gastritis
increasing permeability to peptic digestion
ulcer formation

 Chronic gastritis – gastric atrophy
-mucosa gradually becomes atrophic until
little or no gastric gland activity remains
-autoimmune
- leads to achlorhydria and pernicious
anemia

 Peptic ulcer – excoriated area of the mucosa caused
by digestive action of gastric acid
- most common site – first few cm. of duodenum


 Basic cause of peptic ulcer:

1. imbalance between rate of secretion of gastric
juice and degree of protection by gastroduodenal
mucosal barrier
2. degree of neutralization of gastric acid by duodenal
juice

Peptic ulcer
 treatment 1. reduction of stressful condition
2. antacid drugs
3. H2 blocker
4. stop smoking
5. removal of specific cause like
aspirin and alcohol

surgical treatment—vagotomy antrectomy
DISORDER OF SMALL INTESTINE
 Abnormal digestion of food in the small intestine is due to pancreatic failure

1. pancreatitis
2. blockage of pancreatic duct
3. after surgical removal of pancreatic
head
Malabsorption of the small intestine mucosa
1. non tropical sprue -results from toxic effects of
gluten

present in certain grains destruction of
microvilli decreasing absorptive capacity

2. tropical sprue -inflammation of the mucosa,
3. malabsorption sprue- impaired fat absorption
initially
in severe case absorption of other nutrients
are also impaired
DISORDER OF LARGE INTESTINE
 Constipation – slow movement of feces
- large quantities of hard and dry feces in
descending colon
- causes- irregular bowel habit
- inhibition of the defecation reflex weakens the
reflex leading to atony of the bowels


Megacolon- hirschsprung disease
- lack or deficiency of ganglionic cells in the
myenteric plexus
-no defecation reflex
-no peristaltic motility
-severe constipation- accumulation of feces-
distention and rupture

 Diarrhea—rapid movement of fecal material thru large intestine

 Causes--
1.enteritis-virus and bacteria in the intestine
-irritation of the mucosa- increase in
secretion and motility
- defense mechanism
2. psychogenic—periods of nervous tension
- excites parasympathetic nervous
system increasing secretion and
motility

PARALYSIS OF DEFECATION REFLEX IN SPINAL CORD INJURY
 DEFECATION –normally is initiated by movement of feces to
the rectum

-this causes cord mediated defecation reflex
passing from the rectum to the spinal cord and
back to descending,sigmoid colon, rectum and anus

Spinal cord injury
—blocks defecation reflexthis reflex


- destruction of conus medullaris of the spinal cord
destroy the sacral center in which the reflex is
integrated—paralyzing defecation reflex


 Support measures for loss of defecation reflex
-cathartics and enemas

GENERAL DISORDERS OF THE GIT
 VOMITING—means by which GIT rids itself of its contents
when it is irritated over distended or over excitable
-impulse is transmitted by vagal and sympathetic
afferent fibers to the vomiting center in the medulla
-motor response via 5,7,9,10 and 12th cn

 Antiperistalsis—prelude to vomiting
-abdominal contents can be pushed back to the
duodenum –the resulting distention excites vomiting
relfex
 The vomiting act:
1.deep breath
2.raising of the hyoid bone and larynx-opening of lower
esophageal sphincter
3.closure of glottis
4. lifting of soft pallate-closing the post. Nares
5.strong donwward contraction of the diaphragm
6.contraction of abdominal muscle-building intragastric
pressure
7.relaxation of lower esophageal sphincter
8.expulsion of gastric contents
 NAUSEA—conscious recognition of a subconscious
excitation in an area closely associated with
or a part of vomiting center

 causes
1. impulses from the GIT
2. impulses from the lower brain
3. impulses from cerebral cortex

GASTROINTESTINAL OBSTRUCTION
 Can occur at any point along the course of GIT
 Causes
1. malignancy
2. fibrotic constriction from ulceration or peritoneal
adhesion
3. spasm of a segment of GIT
4. paralysis

Abnormal consequence depends on point of obstruction
--obstruction of small intestine
losses of electrolytes and water—plasma loss
circulatory shock
GASSES IN THE GIT AND FLATUS
 From swallowed air
 From bacterial action
 Diffusion from blood

 Stomach—swallowed air
-nitrogen, oxygen
-belching
 Large intestine—bacterial action
-carbon dioxide,methane and hydrogen
-certain food act as substrate for bacteria
thus more air production

slides on reflexes, DTR

Muscle spindle
• A small, complex spindle-shaped sensory receptor located in skeletal muscle
• senses muscle stretch
• consists of several modified muscle fibres, called intrafusal fibres

• The ends of these fibres are contractile
• central portion is non-contractile and innervated by special neurones/gamma motor neurones).
Basic reflexes:
The myotatic(stretch) reflex
The inverse myotatic reflex
The flexion withdrawal-crossed extensor reflex
Motor outputs
Involuntary
Stereotyped
Elicited by specific sensory inputs
The stretch reflex
Designed to maintain muscle length
-by countering a muscle stretch
-with a muscle contraction
Provides the basis for muscle tone
Also called deep tendon reflexes
-rapid, passive muscle stretch activates muscle spindles
-spindle afferents (oarticularly Ia) send impulses to the spinal cord
-connections to homonymous muscle alpha neurons: Monosynaptic
-connections to synergistic muscle alpha motor neurons; monosynaptic
--cause the stretched muscle to contract
Connection to the antagonist muscle thru inhibitory neuron—decreases activity of the antagonist muscle
Inverse myotatic reflex
Designed to control muscle tension
-by countering a muscle contraction with relaxation
-plus contraction of the antagonist mmuscle
Allows controlof muscle force

The flexion withdrawal and crossed extensor reflexs
Designed to withdraw one limb from a painful stimulus, while extending the cnotralateral limb for support

Reflexes ;window into the nervous system
- is sensory pathwayintact?
- -is motor output pathway intact?
deep tendon reflexes:

-present normally
-weak of absent with posterior root, LMN, or anterior root lesion,
-weak or absent with acute UMN lesion
-increased with chromic UMN lesion
Some DTRs often tested;
-biceps(C5-6)
-triceps(C7)
Patellar (knee jerk;L3-4)
-achilles (ankle jerk reflex;S1)

Superficial reflexes;
Present normally
-weak or absent with posterior root, LMN< or anterior root lesion,
-weak of absent with UMN lesion
-relfexes testet; abdominal and cremasteric

Plantar reflex
Present normally
Absent with posterior root, LMN, or anterior root lesion
With UMN lesion, plantar flexion is replaced by extensor plantar response(up-going-toes)
-called babinski reflex
Indicates damage to corticospinal tract
-a remnant nociceptive avoidance reflex

Clonus
-rythmic contractions and relaxations of amuslce grup
-often accompanies increased DTRs seen with UMN damage
bIceps brachii(C5)
=purpose – to provoke a root (C5) or cord(cns)sign
-positive response
-hypoactive (root)
Hyperactive (cord-cns)
Brachioradialis(c6)
Positiveresponse
-hypoactive- root
Hyperactive – cord- cns
Triceps (c7)
Hypoactive root
Hyperactive – cord –cns
Quadriceps(L4)
Hypoactive –root

Hyperactive—cord—cns
Gastroc-soleus(S1)
Hypoactive –root
Hyperactive—cord –cns
In general

reflexes are not pathological if symmetric unless they are absent or hyperreflexic

Assymetry of reflexes and absent reflexes tend to localize to a peripheral nervous system process
Increased reflexes tend to indicate a problem of the central nervous system
Reflexes are routinely tested on neuro exam and are nonspecific as to the etiology of the disease process if abnormal.

They provide information to help localize the problem

the pupillary reflex or pupillary light reflex

is the reduction of pupil size in response to light.

It is a normal response and dependent on the function of the optic nerves and oculomotor nerves
Lack of the pupillary reflex or an abnormal pupillary reflex
can be caused by
optic nerve damage
oculomotor nerve damage
brain death
and depressant drugs
such as barbiturates
The optic nerve is responsible for the afferent limb of the pupillary reflex, or in other words, senses the incoming light.

The oculomotor nerve is responsible for the efferent limb of the pupillary reflex; in other words, it drives the muscles that constrict the pupil.
Dependent on how the pupils constrict or do not constrict one can determine which of the cranial nerves is damaged.

spinal myotatic reflexes

reflexes are the most objective part of neurologic examination and are very helpful in determining the level of damage in the nervous system

http://www.brainviews.com/abFiles/AniPatellar.htm

copy-paste this link on your address bar for the lecture slides on reflexes
https://rcpt.yousendit.com/658035026/428c6f678387972cd4136a3e69aa4e82

link to animation of stretch reflex for further info:
http://trc.ucdavis.edu/biosci10v/bis10v/media/ch25/stretch_reflex_v2.html

its GIT tutorial

The physiology of Gastrointestinal tract can easily be studied and reviewed in these sites/links

Copy paste this link into your address bar cause the web prompter of this blog seemed to have conked out. Once in the webpage scroll to GIT or digestive system and open the specific topic to take the online test. It is advisable to review the animation of the same topic before proceeding to the test question. You will learn and have fun too!

www.mhhe.com/biosci/ap/vdghumananatomy/student/olc2/ap_animation-quizzes.html

digestion and absorption of fats
http://bcs.whfreeman.com/thelifewire/content/chp50/5002001.html

more animation on digestion
http://highered.mcgraw-hill.com/sites/0072495855/student_view0/chapter26/animation__organs_of_digestion.html

Botulinum toxin

Mr Gaitano during the discussion of Clostridium botolinum, a gm+ bacilli has asked about the use of this toxin medically.

The popular use of BOTOX treatment must be the subject Gaitano was asking about. Botox is afterall botulinum toxin and is used for its capacity to block acetylcholine release at motor-end-plate. If we could recall, the acetylcholine vesicles in the nerve terminal need to bind with the presynatic membrane so that it can be released by exocytosis. This is the precise process that is being block by the toxin. The inhibition of acetylcholine release then results in loss of impulse conduction to the sarcolemma and thus lost of muscular contractility or tone. This is seen as flaccid paralysis in the affected musculature.

Thus it is this action that the toxin is used for treatment of spastic muscular conditions.

http://emedicine.medscape.com/article/325451-overview

check gm- organisms lecure slides at january 08 posting

energetics

only miss Tiongko is energetic in energetics

more on ETC and ATP synthase

http://bcs.whfreeman.com/thelifewire/content/chp07/0702001.html

set point of temperature regulation

how does the body control its temperature? There is a set point temperature from deep tissues which other parts of the body have to follow. Peripheral temperature that is either above or below the set point will trigger body reflex mechanisms to facilitate heat-loss or heat conservation.

how? check this out
http://www.brown.edu/Courses/BI0020_Miller/week/10/web-2/4-2-2007_10-21-10/Chapter_41/Present/Animations/41_A02/41_A02s.html

body thermostat

http://bcs.whfreeman.com/thelifewire/content/chp41/41020.html

back to staining

Gram staining has to do with:

peptidoglycan in the cell wall

basic dyes and its chromophore

a mordant dye to form dye-iodine complex

find out here

http://www2.muw.edu/~lbrandon/Micro/simple.doc

to see is to believe -check this animation

http://www.microbelibrary.org/microbelibrary/files/ccImages/Articleimages/keen/Gramstainkeen.htm

korean tops microlab exam

1. PARK
2. LIM
3. BLASURCA

A1 performance in physiology

according to scores
1. ROSALES
2. GAITANO
3. OGACION
4. ALAVE
5. NGO
6. LIM
7. ESCONDO

micropath lecture slides

please check on january08 posting